It has been recognised for over 200 years that epicardial coronary arteries may be crossed by muscular bands for limited segments of their courses.1 The term myocardial bridge was first employed in 1961 in a case report describing angiographic systolic narrowing.2 Opinion remains divided as to whether myocardial bridges have pathological consequences or are merely epiphenomena. The clinical consequences of myocardial bridges are difficult to evaluate and invoking the presence of a myocardial bridge as a cause of myocardial ischaemia remains not wholly respectable in the view of many cardiologists. On the one hand a wide range of clinical problems, including acute coronary syndromes and arrhythmias, have been reported in patients whose sole apparent cardiac abnormality is the presence of a myocardial bridge.2,3 Conversely, myocardial bridges may be identified in asymptomatic individuals, there seems little correlation between the severity of systolic narrowing and clinical outcome, and doubts remain about the pathophysiological relevance of a purely transient systolic narrowing of a coronary artery when the predominant phase of coronary blood flow occurs in diastole. The answer to this conundrum is likely to be that at some times, in some patients, some muscle bridges may cause clinically relevant problems. What is required to guide therapy are methods of assessment to identify those bridges that may cause ischaemia.
The last decade has seen advances in invasive technology that have improved the ability to measure both anatomical and physiological parameters of coronary vessels. The use of these techniques in patients with muscle bridges has improved our understanding of the pathophysiology of this interesting condition.